期刊
JOURNAL OF VIROLOGY
卷 87, 期 2, 页码 708-715出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.02118-12
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资金
- PHS from the NIAID, NIH [R01 AI 64060-08, R37 AI51231-11, R01 AI071906-03]
- Clinical Translational Science Award Program, NIH NCRR [UL1 TR000454]
- Fogarty International Center [D43 TW001042]
- International AIDS Vaccine Initiative (IAVI)
- Virology Core at the Emory Center for AIDS Research [P30 AI050409]
- IAVI Protocol C research network
- Yerkes National Primate Research Center [2P51RR000165-51]
- FOGARTY INTERNATIONAL CENTER [D43TW001042] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR000454] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [P51RR000165] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI071906, R01AI064060, R01AI051231, R37AI051231, P30AI050409] Funding Source: NIH RePORTER
In HIV-1 infection, the early set-point viral load strongly predicts both viral transmission and disease progression. The factors responsible for the wide spectrum of set-point viral loads are complex and likely reflect an interplay between the transmitted virus and genetically defined factors in both the transmitting source partner and the seroconverter. Indeed, analysis of 195 transmission pairs from Lusaka, Zambia, revealed that the viral loads in transmitting source partners contributed only similar to 2% of the variance in early set-point viral loads of seroconverters (P = 0.046 by univariable analysis). In multivariable models, early set-point viral loads in seroconverting partners were a complex function of (i) the viral load in the source partner, (ii) the gender of the seroconverter, (iii) specific HLA class I alleles in the newly infected partner, and (iv) sharing of HLA-I alleles between partners in a transmission pair. Each of these factors significantly and independently contributed to the set-point viral load in the newly infected partner, accounting for up to 37% of the variance observed and suggesting that many factors operate in concert to define the early virological phenotype in HIV-1 infection.
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